Molecular biology reports · 2026
DHRS2 regulates epithelial-mesenchymal transition in breast cancer cells.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Karaca Hümeyra, Yaylaz Burcu Salman, Zarerajabi Vahideh, Punar Şeyma, Ekmekci Sema Sirma, Abaci Neslihan
Аннотация
OBJECTIVE: Breast cancer is the most common malignancy among women, and metastatic cases have a significantly poorer prognosis than non-metastatic disease. Epithelial-mesenchymal transition (EMT), characterized by the acquisition of mesenchymal features and enhanced migratory capacity by epithelial cells, is a key mechanism underlying cancer metastasis. DHRS2 has recently gained attention for its role in proliferation, invasion, and apoptosis in breast cancer. This study aimed to investigate the relationship between DHRS2 and EMT-related genes in breast cancer.
METHODS AND RESULTS: DHRS2 was overexpressed in MCF7 breast cancer cells using a liposomal transfection agent, while a knockout model was generated using a lentivirus-mediated CRISPR-Cas9 system. Overexpression was confirmed by RT-PCR, whereas knockout was validated by Sanger sequencing and Western blot analysis. Following genetic modifications, EMT-related gene expression levels were analysed by RT-PCR and compared with wild-type MCF7 cells. Altered DHRS2 expression significantly affected the expression of WNT3A, WNT4, TMED9, and SDC1. These findings suggest that DHRS2 regulates EMT through the Wnt/β-catenin signalling pathway. In addition, the limited changes observed in certain EMT markers indicate that DHRS2 may promote cell migration through partial EMT rather than complete EMT.
CONCLUSION: DHRS2 may influence cellular fate and metastatic potential by regulating EMT processes through multiple signalling pathways, particularly Wnt/β-catenin signalling.
METHODS AND RESULTS: DHRS2 was overexpressed in MCF7 breast cancer cells using a liposomal transfection agent, while a knockout model was generated using a lentivirus-mediated CRISPR-Cas9 system. Overexpression was confirmed by RT-PCR, whereas knockout was validated by Sanger sequencing and Western blot analysis. Following genetic modifications, EMT-related gene expression levels were analysed by RT-PCR and compared with wild-type MCF7 cells. Altered DHRS2 expression significantly affected the expression of WNT3A, WNT4, TMED9, and SDC1. These findings suggest that DHRS2 regulates EMT through the Wnt/β-catenin signalling pathway. In addition, the limited changes observed in certain EMT markers indicate that DHRS2 may promote cell migration through partial EMT rather than complete EMT.
CONCLUSION: DHRS2 may influence cellular fate and metastatic potential by regulating EMT processes through multiple signalling pathways, particularly Wnt/β-catenin signalling.